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  • Behavioural Neurology (1992), 5, 3-10

    Obsessive-compulsive symptoms in neurologic disease: a review

    M.S. George, J.A. Melvin and C.H. Kellner

    Departments of Neurology, and Psychiatry and Behavioral Sciences, Medical University of South Carolina, 171 Ashley Avenue, Charleston, SC 29425-0742, USA

    Correspondence: Dr M.S. George, Senior Staff Fellow, NIMH, Bldg 10, Rm 3N212, 9000 Rockville Pike Road, Bethesda, MD 20892, USA

    Obsessive-compulsive disorder (OCD) is an increasingly recognized disorder with a prevalence of 2-3% (Robins et al., 1984). Once thought to be psychodynamic in origin, OCD is now generally recognized as having a neurobiological cause. Although the exact pathophysiology of OCD in its pure form remains unkown, there are numerous reports of obsessive-compulsive symp- toms arising in the setting of known neurological disease. In this paper, we review the reported cases of obsessive-compulsive symptoms associated with neurologic diseases and outline the known facts about the underlying neurobiology ofOCD. Finally, we synthesize these findings into a proposed theory of the pathophysiology of OCD, in both its pure form and when it accompa- nies other neurological illness.


    Sigmund Freud in his legendary case, The Rat Man, described a patient with obsessive-compulsive symp- toms. Freud speculated that these symptoms arose from some underlying neurotic conflict (Freud, 1959). How- ever, OCD has proven to be refractory to individual psychotherapy (Jenike et al., 1986). Within the past dec- ade substantial evidence has emerged that OCD can be effectively treated with behavioral therapy and potent new serotonergic agents. Concurrently there has been a resurgence of interest in the underlying neurobiOlogy of this interesting disorder.

    It is likely that patients who suffer from OCD symptoms represent a spectrum of diseases, much as the symptoms of parkinsonism can arise from Parkinson's disease (idio- pathic) or other brain pathology. In one form, OCD is idio- pathic, has a marked genetic component, and is sometimes associated with tics or Gilles de la Tourette's syndrome. Other patients with OC symptoms suffer from various neurologic and metabolic illnesses (symptomatic OCD). The literature reports of OCD or obsessive-compulsive symptoms in neurologic diseases are examined below. The underlying pathophysiology of OCD is explored in light of these associations and case reports.


    As described by DSM III-R, obsessive-compulsive dis- order occurs in patients with recurrent obsessions or com- pulsions severe enough to cause marked distress and

    © 1992 Rapid Communications of Oxford Ltd

    interference with their normal routine (APA, 1987). Obsessions are persistent ideas, thoughts, impulses, or images that are intrusive and senseless. The person recog- nizes that the obsessions stem from his own mind and are not imposed from without. Commonly, these obsessions consist of repetitive thoughts of violence, contamination or doubt. Compulsions are repetitive, purposeful and intentional behaviors that are often performed in response to an obsession. The patient normally recognizes that this behavior is excessive or unreasonable. Compulsions com- monly involve handwashing, counting, checking, or touching. As a person attempts to resist a compulsion, a sense of mounting inner tension arises.


    What areas of the brain are important in regulating this abnormal behavior? To begin to answer this question one can study the case reports of OCD patients who had con- commitant brain tumors or infarcts--clear evidence of focal CNS damage that might explain the OCD behavior. There are several reported cases of patients who develop- ed obsessive-compulsive symptoms and were later found to have cerebral tumors. Brickner et al. (1940) described patients with temporal and frontal lobe tumors and seiz- ures who developed obsessive-compulsive symptoms. Seibyl et at. (1989) recently reported an OCD patient with

    Behavioural Neurology. Vol 5 . 1992 3

  • a right frontal meningioma. A patient with a frontal callo- sal tumor developed obsessive-compulsive symptoms consisting of excessive writing (Cambier et al., 1988). Thus, tumors of the frontal or temporal lobes can some- times produce OC symptoms.

    The same is true for infarcts and atrophy. Tonkonogy and Barriera (1989) described a patient with progressive right-frontal lobe and bilateral caudate atrophy who had fears of contamination and compulsive hand-washing. Weilburg et al. (1989) reported a patient with obsessive- compulsive disorder who, on MRI scan, had a unilateral left-sided abnormality in the head of the caudate nucleus and putamen. This was accompanied by EEG slowing. The presumed etiology of this abnormality was ischemia secondary to perinatal anoxia. McKeon et al. (1984) described four cases of obsessive-compulsive disorder following head injury. Hillbom (1960) described a series of closed head injury patients who later developed OCD. Neither of these latter two studies found localizable brain pathology on cranial CT scans.


    Infections directly or indirectly involving the basal gan- glia have been reported in association with obsessive com- pulsive behavior. The most notable examples are the Von Economo's encephalitis cases of the 1920s and 1930s (Jel- life, 1929). Schilder (1938) described several patients recovering from this encephalitis of unknown etiology. During recovery, patients developed obsessions and com- pulsions accompanied by various movement disorders. They had facial rigidity and mask-like faces with accompanying flexor rigidity in the arms. This led Schil- der (1938) to speculate that "it is obvious that the organic disease of the central nervous system is an indispensable factor in the genesis of the psychic symptoms which have been mentioned". In looking at the spectrum of obsessive compulsive disorder, Schilder speculated that approxi- mately one-third of OCD patients had a structural brain etiology. In another third there was a strong hint of an organic background and in the final third there was an unknown cause of the OCD symptoms. Wohlfart et al. (1961) reported a case of compulsive shouting (klazoma- nia) that was associated with oculogyric spasms in a patient who had suffered epidemic encephalitis. The shouting attacks lasted an hour and were accompanied by a normalEEG.

    Recently, Swedo et al. (1989a) interviewed rheumatic fever patients with or without Sydenham' s chorea. Syden- ham's chorea is a movement disorder which follows rheu- matic fever (10-30%) presumably when anticaudate antibodies are formed (Husby et al., 1976). When com- pared with patients who only had rheumatic fever, the

    4 Behavioural Neurology. Vol 5 • 1992


    Sydenham's chorea patients scored significantly higher on criteria for obsessive-compulsive disorder. The authors argue that this lends evidence to a basal ganglia dysfunc- tion theory of the etiology of OCD. A case report by Laplane et aI., (1981) follows this same thinking of infec- tion causing damage to the basal ganglia with resultant OC behavior. Their patient developed obsessive-compulsive symptoms following a wasp sting which produced second- ary necrosis of the basal ganglia.


    In addition to OC symptoms associated with known infec- tions or CNS lesions, there are many examples of obsess- ive-compulsive symptoms arising in the setting of other systemic neurologic disorders. George et al. (1989) reported a patient with multiple sclerosis and obsessive- compulsive disorder. The patient's cranial CT scan showed diffuse peri ventricular white matter lesions. Schwab et al. (1951) noted that many of their Parkinso- nism patients, some of whom had post-encephalitic Par- kinsonism, also had obsessive-compulsive disorder. Their obsessions were often sudden and paroxysmal and subsided after 15-30 min. Lees et al. (1989) recently reviewed the neurobehavioral abnormalities found in Par- kinson's disease and concluded that there was a strong relationship between Parkinson's disease and some of the psychomotor retardation seen in obsessive-compulsive disorder.


    Some authors have examined whether there is an increased rate of perinatal abnormalities in patients who develop obsessive-compulsive disorder. For example, Capstick and Seldrup (1977) compared 33 OCD patients to 33 psychiatric controls. Eleven OCD patients self- reported a history of abnormal birth, whereas only two from the other group gave a similar story. These findings are interesting, but hard to assess due to the problems of being retrospective self-report studies, with mixed psychi- atric patients as controls.


    Some authors have remarked that many of the interictal personality changes seen in patients with temporal lobe epilepsy (TLE) resemble behaviors seen in obsessive compulsive disorder (Bear and Fidio, 1977; Blumer, 1975; Bruens, 1969; Waxman and Geschwind, 1975; Ciesielski et al., 1981; Epstein and Bailine, 1971). They proposed that obsessionalism might be a specific consequence of a repeatedly-firing temporal epileptic focus. Kettle and


    TABLE I. Obsessive--compulsive symptoms in neurologic disease

    References ------.---- Lesions Tumors Temporal lobe

    Right Frontal Frontal Caudate